Case Report: Sympathetic crashing acute pulmonary edema – only “NIV and nitroglycerin”?
DOI:
https://doi.org/10.31247/agnj.v2iS1.51Keywords:
Pre-hospital emergency medicine, SCAPE, Sympathetic crashing pulmonary edema, Nitroglycerin, Urapidil, NIV, Non-invasive ventilationAbstract
Introduction An 84-year-old male patient alerted EMS because of severe dyspnea and subsequently presented with respiratory failure due to sympathetic crashing acute pulmonary edema (SCAPE.) The term SCAPE was coined outside Europe, with guidance on treatment only reflecting drugs available in the US and omitting potentially effective options, as highlighted in this report.[1]
Diagnostic findings The patient presented sweating, pale and tachypneic with auscultatory crackles, radial pulse was palpable. He was able to follow commands, but unable to communicate verbally due to dyspnea. Initial SpO2 showed 80%, NIBP 185/105mmHg. The patient described sudden onset dyspnea as the only symptom. An ECG showed sinus tachycardia and LBBB (SGARBOSSA negative.) ABG showed hypoxemia and acidosis due to hypercapnia and lactatemia.
Main diagnosis In absence of other causes for flash pulmonary edema, SCAPE was suspected.
Therapeutic interventions The patient was supported in sitting position, oxygen applied, a total of 25mg urapidil and 7mg morphine administered intravenously, non-invasive ventilation (CPAP+ASB, PEEP 5mbar, ΔASB 5mbar) initiated and an arterial line placed for invasive blood pressure measurement and ABG.
Outcome While RSI was considered multiple times, the patient improved rapidly during transport and a short NIV duration at the emergency department and was transferred to the ward without further interventions.
Discussion With reducing afterload as main goal of pharmacological therapy, urapidil could be as effective as high-dose i.v. nitroglycerine, which is currently recommended.[2,3] While lacking the effect of venous vasodilation and thus not reducing preload, its effect on sympathetic tone via 5-HT1A-receptors supplemental to affecting arterial vasodilation via α-receptors might make it equally effective while being easier to administer. No data is available comparing urapidil to high-dose nitroglycerin, while it has proven more effective than low-dose nitroglycerin.[4]
References
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Houseman BS, Martinelli AN, Oliver WD, Devabhakthuni S, Mattu A. High-dose nitroglycerin infusion description of safety and efficacy in sympathetic crashing acute pulmonary edema: The HI-DOSE SCAPE study. Am J Emerg Med 2023;63:74–8. https://doi.org/10.1016/j.ajem.2022.10.018.
McDonagh TA, Metra M, Adamo M, Gardner RS, Baumbach A, Böhm M, et al. 2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failureDeveloped by the Task Force for the diagnosis and treatment of acute and chronic heart failure of the European Society of Cardiology (ESC) With the special contribution of the Heart Failure Association (HFA) of the ESC. Eur Hear J 2021;42:ehab368. https://doi.org/10.1093/eurheartj/ehab368.
Schreiber W, Woisetschläger C, Binder M, Kaff A, Raab H, Hirschl MM. The nitura study — effect of nitroglycerin or urapidil on hemodynamic, metabolic and respiratory parameters in hypertensive patients with pulmonary edema. Intensiv Care Med 1998;24:557–63. https://doi.org/10.1007/s001340050615.
